Many implantable medical devices (IMDs) have been developed over the years for clinical implantation in patient's bodies that deliver electrical stimulation to a body organ, muscle, nerve or brain cells. Each year approximately 750,000 patients develop bradycardia symptoms such as dizziness, extreme fatigue, shortness of breath, or fainting spells. These symptoms are caused by abnormally slow or irregular heart rate, and the most effective method to relieve these symptoms is to implant a pacing system that generates and delivers pacing pulses to a site in or adjacent to a heart chamber. Pacing systems are incorporated into a wide variety of implantable pacemakers and also into implantable cardioverter defibrillators (ICDs). Such pacing systems comprise an implantable pulse generator (IPG) and one or more lead interconnecting the IPG circuitry with pace/sense electrodes implanted against or into the myocardium of the heart.
Each heart cell contains positive and negative charges due to the selective permeation of certain ions, such as potassium and sodium through the cell membrane. When the cell is at rest, the inside of the cell is negatively charged with respect to the outside. The negative charge is dissipated when the cell is disturbed by an electrical signal that causes the permeability of the cell membrane to change and allows the ingress of positive charge ions. The resulting dissipation of the negative charges constitutes the “depolarization” of the cell. Simultaneously, the cell contracts causing (in conjunction with the contraction of adjoining cells) the heart muscle to contract. Thus, the stimulation of the heart muscle affects both the depolarization and the contraction of the once-polarized myocardial cells that make up the muscle.
Following depolarization and contraction of a heart cell, the “repolarization” or recovery of the cell commences so that the cell is ready to respond to the next applied stimulus. During the repolarization time interval, the cell membrane begins to pump out the positive-charged ions that have entered following the application of the stimulus, that is, during the depolarization of the cell. As these positive charges leave, the inside of the cell membrane starts to become negative again, the cell relaxes, and the potential difference builds up again.
The individual myocardial cells are arranged to form muscle fibers and sheets that, in gross, constitute the heart itself. The depolarization of the atrium is characterized by a P-wave viewed on an electrocardiogram (ECG), and depolarization and repolarization signals of the ventricle, are referred to as the QRS complex and the T wave, respectively. The sequence of depolarization, which manifests itself in a contraction of the heart muscle, and repolarization, which manifests itself in the relaxation and filling of the interior chambers of the heart with blood, is accomplished through a system of specialized muscle tissue that functions like a nerve network. Depolarization signals are generated in the SA node of specialized cardiac cells located in the atria at a rate that is appropriate for the body's physiologic demand for cardiac output. The system then conducts these impulses rapidly to all the muscle fibers of the ventricles, ensuring coordinated, synchronized pumping.
When this system fails, or is overridden by abnormal mechanisms, a pacing system may be needed to generate and deliver trains of pacing pulses through pace/sense electrodes to maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart. The pacing circuitry of pacemaker and ICD IPGs is powered by a battery, and each delivered pacing pulse consumes a discrete bolus of the battery energy. Consequently, the IPG longevity is primarily governed by the battery lifetime. Currently, the IPG longevity can range from approximately 3 to 10 years depending on the type of IPG (e.g., pacemaker or ICD). The IPG must be replaced when the battery is depleted, an expensive procedure that also poses significant discomfort and risk to the patient.
The pacing current drawn by each pacing pulse is a major factor that impacts the battery life and device longevity, although its impact is greater for some devices than the others. For example, recently developed bi-ventricular pacing systems incorporated into pacemakers and ICDs present a high current drain since two pacing pulses must be delivered to synchronously pace both ventricles at a pacing rate that typically depends upon the patient's physiologic need for cardiac output as determined by an activity sensor, for example. Thus, the reduction in delivered pacing current would certainly increase the IPG longevity and could allow the battery and corresponding IPG size to be reduced, and therefore positively impact lives of thousands of patients receiving battery powered IMDs.
In the history of implantable cardiac pacemakers, great strides have been made in increasing longevity, reliability, and versatility of IPGs and the associated lead systems. In the early days of implantable cardiac pacemakers, battery depletion was rapid, leading to exhaustion of the IPG batteries within a year from implantation. The high energy consumption was due to a wide variety of factors, including battery self discharge, pace/sense electrode-tissue interface inefficiencies requiring delivery of high energy pacing pulses, and high current consumption by discrete electronic circuit components.
It was recognized from the outset of cardiac pacing that IPG battery current drain is directly proportional to the amount of energy that is necessary when delivered to the heart to cause the heart to depolarize, i.e., to “capture” the heart. Over the last forty years, reliability and longevity have dramatically improved due to improvements in battery technologies, lead and pace/sense electrode technologies, electronic circuitry current consumption and a wide variety of other areas. As improvements in one area led to increased longevity and reliability, attention was focused on the other areas.
In this evolutionary process, early studies were conducted to determine if the optimum stimulation pulse polarity and wave shape could be found that would achieve capture of the heart at the lowest expenditure of pulse energy in order to prolong pacemaker battery life as reported, for example, by Egbert Dekker, M. D., in “Direct Current Make and Break Thresholds for Pacemaker Leads”, (Circulation Research, vol. XXVII, November 1970, pp. 811–823). In the infancy of cardiac pacemakers, experiments were performed using various forms of electrical stimulation pulses including anodal (positive going) and cathodal (negative going) pacing pulses having pulse energy exceeding the stimulation threshold to trigger depolarization of myocardial cells.
Contemporaneously, attention was focused on other factors, particularly pace/sense electrode technologies, high energy density, low self discharge, battery technology, variable pulse energy output pulse circuits, and capture threshold determination techniques that made dramatic improvements in IPG longevity, reliability and size. The pace/sense electrode technologies have included pace/sense electrode materials including substrates, coatings and surface treatments, pace/sense electrode shapes, pace/sense electrode surface areas, and pace/sense electrode configurations as well as minimizing local tissue injury when the pace/sense electrode fixed in place by a tissue penetrating active fixation mechanisms, delivery of steroids to the stimulation site by incorporation of steroid eluting elements in the lead body adjacent to the fixation mechanism or coatings on the fixation mechanism.
Today's implantable pacemakers and pacing systems incorporated into ICDs are far more versatile and offer a wider variety of therapies for medical conditions that were not imagined in the infancy of cardiac pacing. Currently, electrical stimulation generated by a pacemaker or ICD IPG is in the form of pacing pulses typically having a fixed duration in the order of about 0.5 ms, a voltage of less than 5 volts, and a resulting delivered current dependent upon the collective impedance or load that the pulse is delivered through a cardiac lead conductor and the pace/sense electrode-tissue interface at an active pace/sense electrode. The exponential decaying voltage, cathodal (negative going) pacing pulse shape achieved by a relatively simple, monophasic capacitive discharge output circuit has become accepted as the standard pacing pulse for many years.
Thus, a negative voltage pulse is typically delivered at the active pace/sense electrode, whereby the active pace/sense electrode is characterized as a cathode pace/sense electrode and the return or indifferent pace/sense electrode in the discharge path is characterized as an anode pace/sense electrode. A cathodic electrical field of sufficient strength and current density has to be impressed upon the excitable tissue in the vicinity of the active site to initiate conduction of a depolarization wave through the entire cardiac tissue mass of a heart chamber that causes the heart chamber to contract and expel blood from the heart chamber, i.e., to capture the heart. The minimum pacing pulse energy necessary to produce that effect is referred to as the “stimulation threshold” or “pacing threshold.” The greater the efficiency of the cathode in impressing the electric field on the tissue, the smaller is the amplitude and/or duration of the pulse required to exceed the stimulation threshold. With the widespread adoption of multi-programmable parameters including programmable pulse width and amplitude, physicians have become accustomed to determining the patient's pacing threshold and setting the energy level to a minimum value to capture the heart plus an adequate safety margin.
Despite these efforts and realized improvements, a need remains to further reduce pacing thresholds.